Further studies are warranted to determine the ultimate role of BRCA1 haploinsufficiency-driven metabolic reprogramming in the discrete evolutionary pathways occurring in BRCA1-associated breast tumors [94] and whether a similar metabolic facet should be contemplated when assessing the pathophysiology, consequences and therapeutic value of other well-known oncosuppressors. The gene discussed is BRCA1; the disease is breast neoplasm.